Human MutY homolog induces apoptosis in etoposide-treated HEK293 cells | Zendy

Soo-Hyun Hahm | Zendy; Ji Hyung Chung | Zendy; Lia Agustina | Zendy; SE-HEE HAN | Zendy; InSoo Yoon | Zendy; Jong-Hwa Park | Zendy; LinWoo Kang | Zendy; JinWoo Park | Zendy; JONG JOO NA | Zendy; Ye Sun Han | Zendy

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Human MutY homolog induces apoptosis in etoposide-treated HEK293 cells

Author(s) -

Soo-Hyun Hahm,

Ji Hyung Chung,

Lia Agustina,

SE-HEE HAN,

InSoo Yoon,

Jong-Hwa Park,

LinWoo Kang,

JinWoo Park,

JONG JOO NA,

Ye Sun Han

Publication year - 2012

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2012.921

Subject(s) - apoptosis , etoposide , gene knockdown , cell cycle , cancer research , dna damage , microbiology and biotechnology , ataxia telangiectasia , oncogene , hek 293 cells , biology , chemistry , cell culture , biochemistry , dna , genetics , chemotherapy

Etoposide (ETP) treatment of ataxia telangiectasia mutated (ATM) and Rad3-related protein (ATR)-, topoisomerase-binding protein-1 (TopBP1) and human MutY homolog (hMYH)-depleted cells results in a significant reduction in apoptotic signaling. The association between ATR or TopBP1 and hMYH increased following ETP treatment. In hMYH knockdown cells, the interaction between ATR and TopBP1 decreased following ETP treatment. We suggest that hMYH functions as a sensor of ETP-induced apoptosis. The results suggest that in the absence of hMYH, cells are unable to recognize the damage signal and the ATR pathway is not activated.

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